Abstract

Retinal disease can alter both the amplitude and the timing of the a- and b-waves of the ERG. Recently, Hood and Birch¹ proposed a computational model, shown in schematic form in Fig. 1, to relate mechanisms of disease action to changes in the a- and b-waves. Following Granit's analysis, the a- and b-waves result from the algebraic summation of two potentials PIII (called here P3), generated by receptors, and PII (called here P2), generated by cells of inner nuclear layer (INL). A computational model of the receptor response from Hood and Birch²,³ generates P3 and is the input to a P2 generator. The ERG is the sum of the P3 and P2 responses. The model in Fig. 1 was designed to describe changes in the a- and b-waves with changes in the energy of a brief flash. In particular, the model predicts the leading edge of the a-wave, and the implicit time and trough-to-peak amplitude of the b-wave. The changes with disease were captured by changing one or more of the parameters of this model.

© 1992 Optical Society of America